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Hashimoto Thyroiditis in Primary Thyroid Non-Hodgkin Lymphoma.

原发性甲状腺非霍奇金淋巴瘤中的桥本甲状腺炎。

  • 影响因子:2.13
  • DOI:10.1093/ajcp/aqz145
  • 作者列表:"Travaglino A","Pace M","Varricchio S","Insabato L","Giordano C","Picardi M","Pane F","Staibano S","Mascolo M
  • 发表时间:2020-01-02
Abstract

OBJECTIVES:To assess the prevalence of Hashimoto thyroiditis (HT) in primary thyroid lymphoma (PTL) and whether it differs between mucosa-associated lymphoid tissue (MALT) lymphoma and diffuse large B-cell lymphoma (DLBCL). METHODS:Electronic databases were searched for studies assessing HT prevalence in PTL, based on antithyroid antibodies, clinical history, or pathology. Pooled prevalence of HT and its association with histotype (MALT or DLBCL) were calculated. RESULTS:Thirty-eight studies with 1,346 PTLs were included. Pooled prevalence results were 78.9% (any HT evidence), 65.3% (antithyroid antibodies), 41.7% (clinical history), and 64% (pathology). HT prevalence was significantly higher in MALT lymphoma than in DLBCL (P = .007) and in mixed DLBCL/MALT than in pure DLBCL (P = .002). CONCLUSIONS:Overall, 78.9% of patients with PTL have any HT evidence, but only half of these had been clinically followed. The difference in HT prevalence suggests that a subset of DLBCL may not derive from MALT lymphoma.

摘要

目的: 评估桥本甲状腺炎 (HT) 在原发性甲状腺淋巴瘤 (PTL) 中的患病率及其在黏膜相关淋巴组织 (MALT) 中的差异。淋巴瘤和弥漫性大 b细胞淋巴瘤 (DLBCL)。 方法: 根据抗甲状腺抗体、临床病史或病理,检索电子数据库,寻找评估 PTL 中 HT 患病率的研究。计算 HT 的合并患病率及其与组织类型 (MALT 或 DLBCL) 的相关性。 结果: 共纳入 38 个研究,共 1,346 个 PTLs。汇总患病率结果为 78.9% (任何 HT 证据) 、 65.3% (抗甲状腺抗体) 、 41.7% (临床病史) 和 64% (病理)。HT 患病率在 MALT 淋巴瘤中显著高于 DLBCL (P =.007),在混合 DLBCL/MALT 中显著高于纯 DLBCL (P =.002)。 结论: 总体而言,78.9% 的 PTL 患者有任何 HT 证据,但其中只有一半被临床随访。HT 患病率的差异表明,DLBCL 的一部分可能不是来源于 MALT 淋巴瘤。

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影响因子:2.13
发表时间:2020-01-02
DOI:10.1093/ajcp/aqz145
作者列表:["Travaglino A","Pace M","Varricchio S","Insabato L","Giordano C","Picardi M","Pane F","Staibano S","Mascolo M"]

METHODS:OBJECTIVES:To assess the prevalence of Hashimoto thyroiditis (HT) in primary thyroid lymphoma (PTL) and whether it differs between mucosa-associated lymphoid tissue (MALT) lymphoma and diffuse large B-cell lymphoma (DLBCL). METHODS:Electronic databases were searched for studies assessing HT prevalence in PTL, based on antithyroid antibodies, clinical history, or pathology. Pooled prevalence of HT and its association with histotype (MALT or DLBCL) were calculated. RESULTS:Thirty-eight studies with 1,346 PTLs were included. Pooled prevalence results were 78.9% (any HT evidence), 65.3% (antithyroid antibodies), 41.7% (clinical history), and 64% (pathology). HT prevalence was significantly higher in MALT lymphoma than in DLBCL (P = .007) and in mixed DLBCL/MALT than in pure DLBCL (P = .002). CONCLUSIONS:Overall, 78.9% of patients with PTL have any HT evidence, but only half of these had been clinically followed. The difference in HT prevalence suggests that a subset of DLBCL may not derive from MALT lymphoma.

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影响因子:2.24
发表时间:2020-01-08
DOI:10.1007/s00268-019-05337-9
作者列表:["Lee, Inhwa","Kim, Hyeung Kyoo","Soh, Euy Young","Lee, Jeonghun"]

METHODS:Background Whether chronic lymphocytic thyroiditis (CLT) influences the risk of development and the progression of papillary thyroid cancer (PTC) remains uncertain. We investigated the effects of CLT on the clinicopathologic features and prognosis of PTC. Methods Two thousand nine hundred twenty-eight consecutive patients with PTC treated between 2009 and 2017 were divided into two groups: one with chronic lymphocytic thyroiditis and one without; 1174 (40%) of the patients had coincident CLT. Results In univariate analysis, CLT correlated positively with small tumor size, frequent extrathyroidal extension, multifocal diseases, and p53 but negatively with central lymph node (LN) metastasis and BRAF mutation. In multivariate analysis, CLT was associated with extrathyroidal extension and multifocal disease; however, it was not a prognostic factor for recurrence even though it was associated with two aggressive factors. Compared with patients with PTC alone, there were more retrieved central LNs in the PTC + CLT group, and these patients also underwent more invasive diagnostic tests such as fine needle aspiration cytology and frozen biopsy of LN. Conclusions The CLT patients with PTC had better behavior features and prognoses than did those with PTC alone despite frequent multifocality and extrathyroidal extension. However, precaution may be necessary to avoid performing invasive diagnostic procedures for lateral LN metastasis and to manage the patients appropriately.

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影响因子:2.69
发表时间:2020-01-29
DOI:10.1016/j.bbrc.2019.11.047
作者列表:["Zhang Z","Xu T","Qin W","Huang B","Chen W","Li S","Li J"]

METHODS::PTPN2 is one of the members of the protein Tyrosine Phosphatases (PTPs) family. To explore the promotive effect of upregulated PTPN2 induced by inflammatory response or oxidative stress on the progression of thyroid cancer. PTPN2 level in thyroid cancer tissues and cell lines was detected. Kaplan-Meier method was applied for evaluating the prognostic value of PTPN2 in thyroid cancer patients. After stimulation of inflammatory response (treatment of IFN-γ and TNF-α), or oxidative stress (treatment of H2O2), protein level of PTPN2 in K1 cells was measured by Western blot. Regulatory effects of PTPN2 on EdU-positive staining and Ki-67 positive cell ratio in K1 cells either with H2O2 stimulation or not were determined. PTPN2 was upregulated in thyroid cancer tissues and cell lines. Its level was higher in metastatic thyroid cancer patients than those of non-metastatic ones. High level of PTPN2 predicted worse prognosis of thyroid cancer. Treatment of either IFN-γ or TNF-α upregulated protein level of PTPN2 in K1 cells. Meanwhile, H2O2 stimulation upregulated PTPN2, which was reversed by NAC administration. With the stimulation of increased doses of H2O2, EdU-positive staining and Ki-67 positive cell ratio were dose-dependently elevated. Silence of PTPN2 attenuated proliferative ability and Ki-67 expression in K1 cells either with H2O2 stimulation or not. Inflammatory response or oxidative stress induces upregulation of PTPN2, thus promoting the progression of thyroid cancer.

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